Schisandra chinensis acidic polysaccharide partialy reverses acetaminophen-induced liver injury in mice

J Pharmacol Sci. 2019 Jul;140(3):248-254. doi: 10.1016/j.jphs.2019.07.008. Epub 2019 Jul 24.

Abstract

Schisandra chinensis is a hepatoprotective herb that has been used for centuries in China. Polysaccharide is one of the major active components in S. chinensis, which has been reported to improve liver injuries induced by carbon tetrachloride, alcohol, or high-fat diet. In this study, we observed the effects and corresponding mechanisms of the secondary component of Schisandra polysaccharide (acidic polysaccharide, SCAP) on a murine model of severe acute liver injury induced by acetaminophen (APAP). SCAP significantly decreased the serum alanine aminotransferase (ALT), aspartate aminotransferas (AST), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) levels, and was found to alleviate hepatic pathological alterations in the mouse model. Meanwhile, SCAP revealed a protective effects on the liver injury-related enzymes and factors, such as significantly diminished malondialdehyde (MDA) levels and glutathione (GSH) depletion, reduced ratio of B-cell lymphoma-2 (Bcl-2)-associated X protein (Bax)/Bcl-2, prohibited cleaved caspase-3 expression, and elevated the expression of p-AMPK, p-Akt, p-glycogen synthase kinase 3β (GSK 3β), nuclear factor erythroid 2-derived-like 2 (Nrf 2) and heme oxygenase-1 (HO-1) proteins in the liver tissues of the mouse model. In conclusion, we speculated that the protective activities of SCAP on the APAP-induced mouse model of acute liver injury might be related to its antioxidation, anti-inflammation and anti-apoptosis properties.

Keywords: Antioxidation; Hepatoprotection; Polysaccharide; Schisandra chinensis.

MeSH terms

  • Acetaminophen / pharmacology*
  • Alanine Transaminase / metabolism
  • Animals
  • Antioxidants / metabolism
  • Aspartate Aminotransferases / metabolism
  • Caspase 3 / metabolism
  • Chemical and Drug Induced Liver Injury / drug therapy*
  • Chemical and Drug Induced Liver Injury / metabolism
  • Glutathione / metabolism
  • Glycogen Synthase Kinase 3 beta / metabolism
  • Heme Oxygenase-1 / metabolism
  • Interleukin-1beta / metabolism
  • Liver / drug effects
  • Liver / metabolism
  • Male
  • Malondialdehyde / metabolism
  • Mice
  • Mice, Inbred ICR
  • NF-E2-Related Factor 2 / metabolism
  • Oxidative Stress / drug effects
  • Plant Extracts / pharmacology*
  • Polysaccharides / pharmacology*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Schisandra / chemistry*
  • Superoxide Dismutase / metabolism

Substances

  • Antioxidants
  • Interleukin-1beta
  • NF-E2-Related Factor 2
  • Plant Extracts
  • Polysaccharides
  • Proto-Oncogene Proteins c-bcl-2
  • Acetaminophen
  • Malondialdehyde
  • Heme Oxygenase-1
  • Superoxide Dismutase
  • Aspartate Aminotransferases
  • Alanine Transaminase
  • Glycogen Synthase Kinase 3 beta
  • Caspase 3
  • Glutathione